Effects of iodoacetate, mannoheptulose and 3-O-methyl glucose on the secretory function and metabolism of isolated pancreatic islets.

doi:10.1210/ENDO-100-5-1276

Paper

Effects of iodoacetate, mannoheptulose and 3-O-methyl glucose on the secretory function and metabolism of isolated pancreatic islets.

Published May 1, 1977 · W. Zawalich, A. Pagliara, F. Matschinsky

Endocrinology

Q1 SJR score

60

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0

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Abstract

The ability of iodoacetate, mannoheptulose, and 3-O-methyl glucose to alter islet cell metabolism and glucose-stimulated insulin secretion was examined. A method for the sequential analysis of the releasing and fuel function of glucose in isolated islets was applied. Insulin release was measured by radioimmunoassay and the metabolism of glucose by determining the rate of tritiated water production from [5-3H]glucose and lactate accumulation. It was found that iodoacetate, in the range of 0.2-1.0 mM, inhibited the metabolism of glucose linearly while release was not blocked until metabolism was reduced by 30-40%. The KI for both processes, release and metabolism, was the same. Pyruvate did not protect against or reverse the effects of iodoacetate. Mannoheptulose inhibited both release and metabolism half-maximally at about 5 mM when 27.5 mM glucose was used as the stimulatory agent. A mannoheptulose-resistant component of glucose metabolism, amounting to 30% of the maximal rate was observed. 3-O-Methyl glucose had no effect on insulin release but reduced glucose utilization and lactate production from low glucose. The results are discussed in light of the two prevailing hypotheses explaining glucose induced insulin release, i.e., the receptor and the metabolism hypotheses.

In Vitro Study

Study Snapshot

Iodoacetate inhibits glucose metabolism and release in pancreatic islets, while mannoheptulose and 3-O-methyl glucose reduce glucose utilization and lactate production from low glucose levels.

PopulationOlder adults (50-71 years)

Sample size24

MethodsObservational

OutcomesBody Mass Index projections

ResultsSocial networks mitigate obesity in older groups.

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Paper

Effects of iodoacetate, mannoheptulose and 3-O-methyl glucose on the secretory function and metabolism of isolated pancreatic islets.

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References

Citations

3-O-Methyl-D-Glucose Blunts Cold Ischemia Damage in Kidney via Inhibiting Ferroptosis.

OMG protects kidneys from prolonged cold ischemia-caused injuries by inhibiting ferroptosis, suggesting potential clinical applications in cold preservation of donor kidneys.

Impaired glucose signaling as a cause of obesity and the metabolic syndrome: The glucoadipostatic hypothesis

Impaired glucose signaling, similar to leptin deficiency, may contribute to obesity and metabolic syndrome by regulating long-term energy balance and chronically regulating food intake.

Ca2+ Influx Does Not Trigger Glucose-Induced Traffic of the Insulin Granules and Alteration of Their Distribution

Glucose-induced insulin granule traffic and alteration of their distribution are regulated by distinct mechanisms from calcium influx, potentially explaining the potentiating effects of glucose independent of ATP-sensitive K+ channel closure.

Glucose desensitization in INS-1 cells: evidence of impaired function caused by glucose metabolite(s) rather than by the glucose molecule per se.

Long-term exposure to high glucose levels in INS-1 cells leads to impaired function caused by glucose metabolite(s) rather than the glucose molecule itself.

Glucose metabolism and pulsatile insulin release from isolated islets.

Pulsatile secretion in pancreatic islets is regulated by factors other than calcium levels, with metabolic inhibition reducing glucose-stimulated secretion but maintaining pulsatility.